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E-raamat: Multiple Sclerosis, Mad Cow Disease and Acinetobacter

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  • Ilmumisaeg: 19-Nov-2014
  • Kirjastus: Springer International Publishing AG
  • Keel: eng
  • ISBN-13: 9783319027357
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Multiple Sclerosis, Mad Cow Disease and AcinetobacterSuurem pilt
  • Formaat: PDF+DRM
  • Ilmumisaeg: 19-Nov-2014
  • Kirjastus: Springer International Publishing AG
  • Keel: eng
  • ISBN-13: 9783319027357
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The aim of this book is to publicise and bring to a wider audience the concept that the cause of two neurological diseases, namely multiple sclerosis (MS) and “mad cow disease” also known as “bovine spongiform encephalopathy” are related through exposure to a common microbe Acinetobacter which is found in human sinuses, on skin and in the soil. An infection is the cause of a neurological disease in man and in animals. Elevated levels of antibodies to Acinetobacter have been found in multiple sclerosis patients as well as in ruminants who have been described as suffering from “mad cow disease” following exposure to contaminated feed supplements. The overall objective and scope of this book is to inform the audience, the reader, that multiple sclerosis may be linked to a microbe Acinetobacter which carries molecular structures resembling myelin, the outer sheath covering of neurons.

This book explores and advances the concept that two neurological diseases, "mad cow disease" and multiple sclerosis, may be linked through exposure to the common microbe Acinetobacter, which is found in human sinuses, on skin and in the soil.
1 Multiple Sclerosis as a Scientific Problem
1(8)
1.1 Multiple Sclerosis: An Introduction
1(1)
1.2 Clinical Features of Multiple Sclerosis
2(1)
1.3 Laboratory and Radiological Features
3(1)
1.4 The Therapy of Multiple Sclerosis
4(1)
1.5 Molecular Mimicry and Rheumatic Fever
4(1)
1.6 The Properties of the Multiple Sclerosis Problem
5(1)
1.7 King's College Immunology Unit
6(3)
References
7(2)
2 History of the Attempts to Find the Origin of Multiple Sclerosis
9(6)
2.1 Introduction
9(1)
2.2 Multiple Sclerosis Before Charcot
9(1)
2.3 Carswell in London
10(1)
2.4 Cruveilhier in Paris
10(1)
2.5 Charcot at the Salpetriere
10(1)
2.6 Multiple Sclerosis in Other Countries
11(1)
2.7 Microscopy of Multiple Sclerosis Lesions in Edinburgh
11(1)
2.8 Clues from Therapy
12(1)
2.9 A "Eureka Moment" in London
12(3)
References
14(1)
3 The Problem of Bovine Spongiform Encephalopathy also Known as "Mad Cow Disease" in the United Kingdom
15(6)
3.1 First Cases of Bovine Spongiform Encephalopathy in the United Kingdom
15(1)
3.2 Origin of the Disease
16(1)
3.3 Scrapie and Related Diseases
16(2)
3.4 The "Bio-assay" is the Fundamental Flaw in "Transmissible Spongiform Diseases" Research
18(1)
3.5 Conclusions
19(2)
References
19(2)
4 Experimental Allergic Encephalomyelitis as a Model of Multiple Sclerosis
21(6)
4.1 Post-rabies Vaccination Allergic Encephalomyelitis
21(1)
4.2 Rabies as a Neurological Disease
22(1)
4.3 "Experimental Allergic Encephalomyelitis" as an Animal Model of Multiple Sclerosis
23(1)
4.4 Features of Experimental Allergic Encephalomyelitis
24(1)
4.5 Conclusions
25(2)
References
26(1)
5 Bovine Spongiform Encephalopathy: Comparison Between the "Prion" Hypothesis and the Autoimmune Theory
27(10)
5.1 Bovine Spongiform Encephalopathy as an Environmental and Nutritional Problem Involving Cattle
27(1)
5.2 Features of Bovine Spongiform Encephalopathy
28(1)
5.3 The Prion Agent as the Cause of BSE
29(1)
5.4 Difficulties Associated with the Prion Hypothesis
30(1)
5.5 General Theory of Autoimmune Diseases
31(1)
5.6 Experimental Allergic Encephalomyelitis as a Model of BSE
32(1)
5.7 Growth Hormone Injections as a Cause of CJD or EAE
32(1)
5.8 The Autoimmune Theory of BSE
33(1)
5.9 Comparisons Between the Prion Hypothesis and the Autoimmune Theory
33(4)
References
35(2)
6 Molecular Sequences in EAE and BSE Point to Acinetobacter Bacteria
37(8)
6.1 Introduction
37(1)
6.2 Experimental Allergic Encephalomyelitis (EAE) as a Model of an Autoimmune Disease Produced by a Mechanism Involving Molecular Mimicry
38(1)
6.3 The Hypothesis That BSE Is an Autoimmune Disease
39(1)
6.4 Molecular Analysis of Myelin Sequences Point to Acinetobacter Bacteria
39(3)
6.5 Discussion and Conclusions
42(3)
References
43(2)
7 Autoantibodies to Brain Components and Antibodies to Acinetobacter Are Present in Bovine Spongiform Encephalopathy
45(12)
7.1 Introduction: Bovine Spongiform Encephalopathy or "Mad Cow Disease" Could Be Due to Environmental Factors
45(1)
7.2 Computer Analysis of a Short Sequence of Bovine Myelin Suggests "Molecular Mimicry" with 3 Common Bacteria: Acinetobacter, Agrobacterium and Escherichia
46(1)
7.3 Sera from Animals with and Without BSE and from Healthy Animals from an Organic Farm
47(1)
Sera from Animals with and Without BSE Supplied by the Central Veterinary Laboratory of the Ministry of Agriculture, Fisheries and Food (MAFF)
47(1)
Control Sera from an Organic Farm Not Associated with MAFF
48(1)
7.4 Bacterial Cultures, ELISA and Absorption Studies
48(1)
Bacterial Cultures
48(1)
ELISA
48(1)
Absorption Studies
49(1)
7.5 Measurement of Autoantibodies to Brain Components
49(2)
7.6 Measurement of Anti-Bacterial Antibodies
51(1)
7.7 Measurement of Antibodies by Serial Dilutions
51(1)
7.8 Discussion and Conclusions
51(6)
References
55(2)
8 Antibodies to Acinetobacter Bacteria But Not to Other Microbes Are Present in Animals with Bovine Spongiform Encephalopathy
57(10)
8.1 Introduction: Bovine Spongiform Encephalopathy Could Be Caused by Environmental Bacteria
57(1)
8.2 Sera from Animals with and Without BSE and Test Bacteria
58(1)
8.3 Bacterial Cultures, Peptides and ELISA
58(1)
Bacterial Cultures
58(1)
Peptides
59(1)
ELISA
59(1)
8.4 Measurement of Anti-Bacterial Total Immunoglobulins
59(2)
8.5 Measurement of Class Specific Anti-Acinetobacter Antibodies
61(1)
8.6 Measurement of Autoantibodies to Brain Components
62(1)
8.7 Relative Comparison of Immunoglobulin Isotypes
62(1)
8.8 Correlation Coefficient Analysis
63(1)
8.9 Discussion and Conclusions
63(4)
References
65(2)
9 An Ante-Mortem Test for Bovine Spongiform Encephalopathy Involving "Myelin-Acinetobacter-Neurofilaments" (MAN) Tested in 12 Strains of Acinetobacter Bacteria
67(12)
9.1 Introduction: Bovine Spongiform Encephalopathy and Environmental Bacteria
67(1)
9.2 Sera from Animals with and Without BSE, Test Bacteria and Peptides
68(1)
9.3 Antibodies to Acinetobacter Peptides and Autoantibodies to Corresponding Bovine Brain Peptides
69(1)
9.4 An Ante-Mortem Test for BSE
69(2)
9.5 Sensitivity and Specificity of Ante-Mortem Test
71(4)
9.6 Discussion and Conclusions
75(4)
References
78(1)
10 Antibodies to Prion and Acinetobacter Peptide Sequences in Bovine Spongiform Encephalopathy
79(8)
10.1 Introduction: The Possible Link Between Prions and Acinetobacter Bacteria
79(1)
10.2 Materials and Methods: Serum Samples, Peptides and ELISA
80(1)
Serum Samples
80(1)
Peptides
80(1)
ELISA
81(1)
Statistical Studies
81(1)
10.3 The Presence of Molecular Mimicry Between Bovine Prion and Acinetobacter Sequences
81(1)
10.4 Antibodies to Bovine Prion QVYY(RPVDQ)YSNQN Peptide Sequences
81(1)
10.5 Antibodies to Acinetobacter AIGS(RPVDQ)HLKAL Peptide Sequences
82(2)
10.6 Correlation Coefficient Studies
84(1)
10.7 Discussion and Conclusions
85(2)
References
86(1)
11 Antibodies to Acinetobacter and Pseudomonas Bacteria in Multiple Sclerosis Patients
87(10)
11.1 Introduction: Possible Immune Responses to Acinetobacter and Pseudomonas Bacteria in Multiple Sclerosis Patients
87(1)
11.2 Materials and Methods: Serum Samples, Bacteria and ELISA
88(1)
Serum Samples
88(1)
Bacterial Cultures
89(1)
ELISA
89(1)
Statistical Analysis
89(1)
11.3 IgA Anti-Acinetobacter Antibodies in Multiple Sclerosis and CVA Patients
89(2)
11.4 IgG Anti-Acinetobacter Antibodies in Multiple Sclerosis and CVA Patients
91(1)
11.5 IgM Anti-Acinetobacter Antibodies in Multiple Sclerosis and CVA Patients
92(1)
11.6 Antibodies to Pseudomonas aeruginosa
93(1)
11.7 Antibodies to Escherichia coli in Multiple Sclerosis Patients
94(1)
11.8 Correlation Coefficient Analysis
94(1)
11.9 Discussion and Pathological Implications
94(3)
References
95(2)
12 Antibodies to Acinetobacter Peptide Sequences Resembling Myelin and Neurofilaments in Multiple Sclerosis Patients
97(12)
12.1 Introduction: The Role of Antibodies to Myelin in Multiple Sclerosis Patients
97(1)
12.2 Materials and Methods: Serum Samples, Bacteria and ELISA
98(2)
Serum Samples
98(1)
Bacterial Cultures
99(1)
ELISA
99(1)
Statistical Analysis
100(1)
12.3 Antibodies to Acinetobacter 11171 in Different Multiple Sclerosis Groups
100(1)
12.4 Antibodies to Myelin Basic Protein in Multiple Sclerosis and CVA Patients
101(1)
12.5 Antibodies to Neurofilaments in Multiple Sclerosis and CVA Patients
102(1)
12.6 IgG Subclass Antibodies to Acinetobacter Species
102(3)
12.7 Correlation Coefficient Analysis
105(1)
12.8 Pathological Implications: Acinetobacter as a Possible Aetiological Agent in Multiple Sclerosis
105(4)
References
107(2)
13 The Myelin-Acinetobacter-Neurofilament Index in an Attempt to Diagnose Multiple Sclerosis
109(10)
13.1 Introduction: The Need for a Laboratory Test of Multiple Sclerosis
109(1)
13.2 Materials and Methods: Serum Samples, Bacteria and ELISA
110(1)
Serum Samples
110(1)
Bacterial Cultures and ELISA
110(1)
Statistical Analysis
111(1)
13.3 Calculation of the Myelin-Acinetobacter-Neurofilament Index in Multiple Sclerosis Groups
111(1)
13.4 Results of the "Myelin-Acinetobacter-Neurofilament" Index Calculations in Multiple Sclerosis Patients
111(4)
13.5 Intrathecal Production of Antibodies and Acinetobacter
115(1)
13.6 Pathological Implications: Acinetobacter as an Extra-thecal Aetiological Agent in Multiple Sclerosis
116(3)
References
117(2)
14 Antibodies to Short Synthetic Acinetobacter and Pseudomonas Peptide Sequences Resembling Myelin and Neurofilaments in Multiple Sclerosis Patients
119(12)
14.1 Introduction: The Use of Synthetic Peptide Sequences of Myelin and Neurofilaments to Study the Role of Antibodies in Multiple Sclerosis Patients
119(2)
14.2 Materials and Methods: Serum Samples, Peptides and ELISA
121(1)
Serum Samples
121(1)
Peptides
121(1)
Preparation of MOG and MBP
121(1)
ELISA
122(1)
Statistical Analysis
122(1)
14.3 Molecular Mimicry Between MOG and Acinetobacter
122(1)
14.4 Multiple Sclerosis Patients Respond to Bacterial Peptide Sequences
122(1)
14.5 Results to Peptide 1: Antibodies to Acinetobacter 4-carboxy Muconolactone Decarboxylase (QNFISRFAWGEVNSR)
123(1)
14.6 Results to Peptide 2: Antibodies to Pseudomonas aeruginosa γ-carboxy Muconolactone Decarboxylase (QEMITRHAWGDIWTR)
123(1)
14.7 Results to Peptide 3: Antibodies to Myelin Basic Protein (MBP Residues 110--124) (GLSLSRFSWGAGQR)
124(1)
14.8 Results to Peptide 4: Antibodies to Acinetobacter sp 3-oxoadipate CoA-transferase Subunit A. (DSYVFDE LYRAGKIE)
125(1)
14.9 Results to Peptide 5: Antibodies to Myelin Oligodendrocyte Glycoprotein (MOG) (Residues 43--57) (PFSRVVH LYRNGKDQ)
126(1)
14.10 Multiple Sclerosis Patients have Antibodies to Bacterial Acinetobacter/Pseudomonas Peptides
126(5)
References
128(3)
15 Antibodies to Acinetobacter and Myelin in Multiple Sclerosis and Creutzfeldt-Jakob Disease Patients
131(10)
15.1 Introduction: Comparison of Antibodies to Acinetobacter and Myelin in Multiple Sclerosis and Creutzfeldt-Jakob Disease Patients Compared to Other Neurological and Arthritic Conditions
131(1)
15.2 Materials and Methods: Serum Samples, Myelin Basic Protein and ELISA
132(2)
Serum Samples
133(1)
Bacterial Preparations
133(1)
ELISA
133(1)
Statistical Analysis
134(1)
15.3 IgA Anti-Bacterial Antibodies
134(1)
15.4 IgG Antibacterial Antibodies
135(1)
15.5 IgA Anti-Myelin Basic Protein Antibodies
136(1)
15.6 Longitudinal Assessment of IgA Antibacterial Antibodies
137(1)
15.7 Correlation Coefficient Analysis
137(1)
15.8 Discussion
138(3)
References
139(2)
16 Creutzfeldt-Jakob Disease and its Variants
141(12)
16.1 Introduction: The First Descriptions of Creutzfeldt-Jakob Disease
141(1)
16.2 Transmissible Spongiform Encephalopathies
142(1)
16.3 Sporadic-Creutzfeldt-Jakob Disease
142(1)
16.4 Acquired or Iatrogenic Creutzfeldt-Jakob Disease
142(1)
16.5 Genetic Creutzfeldt-Jakob Disease
143(1)
16.6 Variant Creutzfeldt-Jakob Disease
143(4)
16.7 Kuru in the Fore Tribe of New Guinea and Gajdusek
147(1)
16.8 The Role of Inflammation in Creutzfeldt-Jakob Disease
147(1)
16.9 Problems Associated with Variant-Creutzfeldt-Jakob Disease
148(2)
16.10 The Autoimmune Theory as an Alternative Hypothesis to the Prion Theory
150(3)
References
151(2)
17 Sinusitis in Multiple Sclerosis and Acinetobacter
153(8)
17.1 Introduction: The First Descriptions of Upper Respiratory Tract Infections in Multiple Sclerosis
153(1)
17.2 Tonsillectomy and Multiple Sclerosis
153(1)
17.3 Multiple Sclerosis and Infections in Canadian Patients
154(1)
17.4 Multiple Sclerosis Associated with Sinusitis in England
154(1)
17.5 Sinusitis in Scottish Multiple Sclerosis Patients
155(1)
17.6 Reversible Optic Neuritis Following Paranasal Sinusitis
156(1)
17.7 Incidence of Sinusitis in Multiple Sclerosis as Measured by Magnetic Resonance Imaging
156(1)
17.8 Viral and Bacterial Infections Associated with Onset of Multiple Sclerosis
157(1)
17.9 Inflammatory Changes in Acute Optic Neuritis Associated with Paranasal Changes
157(1)
17.10 Infections and Multiple Sclerosis in Italy
158(1)
17.11 Prospective Studies in Dutch Multiple Sclerosis Patients
158(1)
17.12 The Latitude Problem in Multiple Sclerosis and Sinusitis
158(1)
17.13 Acinetobacter Microbes in Nasal Sinuses and Multiple Sclerosis
159(2)
References
160(1)
18 The Theory That Multiple Sclerosis, CJD and BSE are Caused by Acinetobacter
161(12)
18.1 Introduction to the Problem of Multiple Sclerosis, Creutzfeldt-Jakob Disease and Bovine Spongiform Encephalopathy
161(1)
18.2 Neurological Complications Following Rabies Vaccination
162(1)
18.3 From EAE to Multiple Sclerosis via Autoimmunity
163(1)
18.4 The Central Immunological Problem of "Transmissible Spongiform Encephalopathies"
164(1)
18.5 The Yehuda Shoenfeld Conjecture
165(1)
18.6 Acinetobacter as the Causative Agent in Multiple Sclerosis
166(2)
18.7 Creutzfeldt-Jakob Disease and Acinetobacter
168(1)
18.8 BSE, Scrapie and Chronic Wasting Disease of Deer and Elks
168(2)
18.9 Further Studies Are Required
170(3)
References
170(3)
19 The Scientific Method of Sir Karl Popper
173(10)
19.1 Sir Karl Popper, the Philosopher of Science
173(1)
19.2 A Biography of Karl Popper
174(1)
19.3 The Problem of Words and Their Meanings
174(1)
19.4 The Scientific Problem and Its Explanation
175(1)
19.5 Evolutionary Theory of Knowledge
176(1)
19.6 The "World 3" Universe
177(1)
19.7 Bacon, Hume and Popper
178(1)
19.8 Popper's Scientific Method
179(1)
19.9 The Hippocratic Oath, Popper and Medicine
180(3)
References
180(3)
20 Multiple Sclerosis and "Popper Sequences"
183(12)
20.1 Introduction to "Popper Sequences"
183(1)
20.2 Components of a "Popper Sequence"
184(1)
20.3 First Popper Sequence
184(1)
20.4 Second Popper Sequence
185(1)
20.5 Third Popper Sequence
186(1)
20.6 Fourth Popper Sequence
187(1)
20.7 Fifth Popper Sequence
188(1)
20.8 Sixth Popper Sequence
188(2)
20.9 Seventh Popper Sequence
190(1)
20.10 Eighth Popper Sequence
190(1)
20.11 Ninth Popper Sequence
191(1)
20.12 Tenth Popper Sequence
192(1)
20.13 General Conclusions
193(2)
References
193(2)
Index 195
Professor Alan Ebringer, Department of Rheumatology, The Middlesex Hospital UCH School of Medicine and Infection & Immunity Group, Division of Life Sciences, Kings College, London, UK.
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